scholarly journals Pregnancy alters body-core temperature response to a simulated open field in rats

1997 ◽  
Vol 82 (5) ◽  
pp. 1406-1410 ◽  
Author(s):  
James E. Fewell ◽  
Patricia A. Tang
Keyword(s):  
Open Field ◽  
Core Temperature ◽  
Temperature Response ◽  
The Body ◽  
Body Core Temperature ◽  
Sprague Dawley ◽  
Induced Hyperthermia ◽  
Sprague Dawley Rats ◽  
Functional Consequences ◽  
Body Core

Fewell, James E., and Patricia A. Tang. Pregnancy alters body-core temperature response to a simulated open field in rats. J. Appl. Physiol. 82(4): 1406–1410, 1997.—Exposure of a rat to a novel environment (e.g., a simulated open field) induces a transient increase in body-core temperature, which is often called stress-induced hyperthermia. Although pregnancy is known to influence thermoregulatory control, its effect on stress-induced hyperthermia is unknown. Therefore, 24 Sprague-Dawley rats (8 nonpregnant and 16 pregnant) were studied to test the hypothesis that pregnancy would alter the development of stress-induced hyperthermia after exposure to a simulated open field. Body-core temperature index increased significantly after exposure to a simulated open field in nonpregnant and gestation day-10 rats but not in gestation day-15 and day-20 rats. Thus our data provide evidence that pregnancy influences the body-core temperature response of rats exposed to a simulated open field in a gestation-dependent fashion. The functional consequences as well as the mechanisms involved remain to be determined.

scholarly journals Cerebral cortex does not modulate “regulated” decrease in core temperature during hypoxemia in rats

1998 ◽  
Vol 274 (4) ◽  
pp. R1158-R1161
Author(s):  
Evvi-Lynn M. Rollins ◽  
James E. Fewell
Keyword(s):  
Cerebral Cortex ◽  
Core Temperature ◽  
Cortical Spreading Depression ◽  
Spreading Depression ◽  
Temperature Response ◽  
Sprague Dawley ◽  
Adult Rats ◽  
The Core ◽  
Sprague Dawley Rats ◽  
Before And After

In newborns and adults of a number of species including humans, exposure to acute hypoxemia produces a “regulated” decease in core temperature, the mechanism of which is unknown. Considering that various cortical areas participate in autonomic regulation including thermoregulation, the present experiments were carried out to test the hypothesis that the cerebral cortex plays a role in modulating the regulated decrease in core temperature during acute hypoxemia. This hypothesis was tested by determining the core temperature response to acute hypoxemia in chronically instrumented adult Sprague-Dawley rats before and after cortical spreading depression (i.e., functional decortication) was produced by the local application of potassium chloride to the dura overlying the cerebral hemispheres. There was no effect of cortical spreading depression on baseline core temperature. Core temperature decreased during acute hypoxemia in a similar fashion when the cerebral cortex was intact as well as during functional decortication. Thus our data do not support the hypothesis that the cerebral cortex modulates the regulated decrease in core temperature that occurs in adult rats during acute hypoxemia.

Influence of nicotine on the core temperature response to a novel environment in pregnant rats

1997 ◽  
Vol 83 (5) ◽  
pp. 1612-1616 ◽  
Author(s):  
James E. Fewell ◽  
Patricia A. Tang
Keyword(s):  
Open Field ◽  
Core Temperature ◽  
Temperature Response ◽  
Chronic Administration ◽  
Female Rat ◽  
Sprague Dawley ◽  
Pregnant Rats ◽  
Temperature Index ◽  
Novel Environment ◽  
The Core

Fewell, James E., and Patricia A. Tang. Influence of nicotine on the core temperature response to a novel environment in pregnant rats. J. Appl. Physiol.83(5): 1612–1616, 1997.—Exposure of a male or nonpregnant female rat to a novel environment, such as a simulated open field, induces a transient increase in core temperature, which is often called stress-induced hyperthermia. Pregnancy alters this response such that the core temperature index increases significantly during exposure to a simulated open field on day 10 but not on days 15 and 20 of gestation in rats. The present experiments were carried to investigate the effect of chronic administration of nicotine (0, 1, 2, 4, or 8 mg ⋅ kg−1 ⋅ 24 h−1 for 13–15 days) on the core temperature response to a simulated open field in chronically instrumented pregnant ( day 20 or 21 of gestation) and nonpregnant Sprague-Dawley rats. In nonpregnant rats, the core temperature index increased more during exposure to a simulated open field after chronic administration of nicotine at all doses than after chronic administration of vehicle; the core temperature response was not dependent on the dose of nicotine. In pregnant rats, significant increases in core temperature as well as in the core temperature index occurred only during exposure to a simulated open field after chronic administration of nicotine in doses of 2, 4, or 8 mg ⋅ kg−1 ⋅ 24 h−1; the core temperature response was dependent on the dose of nicotine. Our data provide evidence that chronic exposure to nicotine enhances the core temperature response to a simulated open field in nonpregnant rats and unmasks a maternal thermogenic response that is not seen to the same stimulus near term of pregnancy. The possible physiological consequences for the fetus are presently unknown and require investigation.

scholarly journals Evaluation of Various Cooling Systems After Exercise-Induced Hyperthermia

2017 ◽  
Vol 52 (2) ◽  
pp. 108-116 ◽  
Author(s):  
Pearl M. S. Tan ◽  
Eunice Y. N. Teo ◽  
Noreffendy B. Ali ◽  
Bryan C. H. Ang ◽  
Iswady Iskandar ◽  
...  
Keyword(s):  
Cooling Rate ◽  
Core Temperature ◽  
Cooling System ◽  
Rating Of Perceived Exertion ◽  
Body Core Temperature ◽  
Cooling Systems ◽  
Induced Hyperthermia ◽  
Objective Evidence ◽  
Body Core ◽  
Exercise Induced

Context: Rapid diagnosis and expeditious cooling of individuals with exertional heat stroke is paramount for survival. Objective: To evaluate the efficacy of various cooling systems after exercise-induced hyperthermia. Design: Crossover study. Setting: Laboratory. Patients or Other Participants: Twenty-two men (age = 24 ± 2 years, height = 1.76 ± 0.07 m, mass = 70.7 ± 9.5 kg) participated. Intervention(s): Each participant completed a treadmill walk until body core temperature reached 39.50°C. The treadmill walk was performed at 5.3 km/h on an 8.5% incline for 50 minutes and then at 5.0 km/h until the end of exercise. Each participant experienced 4 cooling phases in a randomized, repeated-crossover design: (1) no cooling (CON), (2) body-cooling unit (BCU), (3) EMCOOLS Flex.Pad (EC), and (4) ThermoSuit (TS). Cooling continued for 30 minutes or until body core temperature reached 38.00°C, whichever occurred earlier. Main Outcome Measure(s): Body core temperature (obtained via an ingestible telemetric temperature sensor) and heart rate were measured continuously during the exercise and cooling phases. Rating of perceived exertion was monitored every 5 minutes during the exercise phase and thermal sensation every minute during the cooling phase. Results: The absolute cooling rate was greatest with TS (0.16°C/min ± 0.06°C/min) followed by EC (0.12°C/min ± 0.04°C/min), BCU (0.09°C/min ± 0.06°C/min), and CON (0.06°C/min ± 0.02°C/min; P < .001). The TS offered a greater cooling rate than all other cooling modalities in this study, whereas EC offered a greater cooling rate than both CON and BCU (P < .0083 for all). Effect-size calculations, however, showed that EC and BCU were not clinically different. Conclusion: These findings provide objective evidence for selecting the most effective cooling system of those we evaluated for cooling individuals with exercise-induced hyperthermia. Nevertheless, factors other than cooling efficacy need to be considered when selecting an appropriate cooling system.

Restoration of thermoregulation after exercise

2017 ◽  
Vol 122 (4) ◽  
pp. 933-944 ◽  
Author(s):  
Glen P. Kenny ◽  
Ryan McGinn
Keyword(s):  
Heat Loss ◽  
Core Temperature ◽  
Current Knowledge ◽  
Thermal Control ◽  
The Body ◽  
Body Core Temperature ◽  
Whole Body ◽  
Temperature Sensitive ◽  
Internal Core ◽  
Body Core

Performing exercise, especially in hot conditions, can heat the body, causing significant increases in internal body temperature. To offset this increase, powerful and highly developed autonomic thermoregulatory responses (i.e., skin blood flow and sweating) are activated to enhance whole body heat loss; a response mediated by temperature-sensitive receptors in both the skin and the internal core regions of the body. Independent of thermal control of heat loss, nonthermal factors can have profound consequences on the body’s ability to dissipate heat during exercise. These include the activation of the body’s sensory receptors (i.e., baroreceptors, metaboreceptors, mechanoreceptors, etc.) as well as phenotypic factors such as age, sex, acclimation, fitness, and chronic diseases (e.g., diabetes). The influence of these factors extends into recovery such that marked impairments in thermoregulatory function occur, leading to prolonged and sustained elevations in body core temperature. Irrespective of the level of hyperthermia, there is a time-dependent suppression of the body’s physiological ability to dissipate heat. This delay in the restoration of postexercise thermoregulation has been associated with disturbances in cardiovascular function which manifest most commonly as postexercise hypotension. This review examines the current knowledge regarding the restoration of thermoregulation postexercise. In addition, the factors that are thought to accelerate or delay the return of body core temperature to resting levels are highlighted with a particular emphasis on strategies to manage heat stress in athletic and/or occupational settings.

Thermal regulatory dysfunction of growth hormone in classical heat stroke?

1996 ◽  
Vol 134 (6) ◽  
pp. 727-730
Author(s):  
Abdulaziz Alzeer ◽  
Abdullah Al Arifi ◽  
Mohsen El-Hazmi ◽  
Arjumand S Warsy ◽  
Eric S Nylen
Keyword(s):  
Growth Hormone ◽  
Core Temperature ◽  
Heat Stroke ◽  
The Body ◽  
Body Core Temperature ◽  
Treatment Unit ◽  
Gh Secretion ◽  
Body Core ◽  
Time Of Admission ◽  
Regulatory Dysfunction

Alzeer A, Al Arifi A, El-Hazmi M, Warsy AS, Nylen ES. Thermal regulatory dysfunction of growth hormone in classical heat stroke? Eur J Endocrinol 1996;134:727–30. ISSN 0804–4643 Growth hormone (GH) secretion associated with classical (non-exertional) heat stroke (HS) was evaluated in 26 HS victims and 10 control (non heat-exhausted) subjects during the annual Hajj in Makkah, Saudi Arabia. On admission to the HS treatment unit, the GH level was 1.54 ± 0.14 ng/ml (approximately 3.5-fold higher in the HS victims compared to controls; p = 0.005). The GH levels subsequently declined by 78% by 24 h. The categorized GH response was significantly associated with survival for those subjects with a GH level of < 5.53 ng/ml by 6 h (chi-squared test; p = 0.06). In those patients who died (N = 6), there was a continued increase in GH levels from the time of admission, which peaked at 6 h. In those patients who survived, the GH levels peaked at the time of admission and declined rapidly thereafter. There was a direct correlation of age and GH level upon admission (p = 0.02), as well as to peak GH (p = 0.041). However, there was no relationship of GH level to either body core temperature or the cooling time. In summary, HS induced significant GH secretion. The degree of GH response was not related to the body core temperature and was more pronounced in older individuals and in those that died. Although patients with GH deficiency and HS are characterized by anhidrosis/hypohidrosis, there does not appear to be dysfunction of GH response to heat stress-associated HS. In contrast, a vigorous GH response at 6 h suggested a worse outcome. ES Nylen, Rm GE 246, VAMC, 50 Irving St, NW Washington, DC 20422, USA

Keeping a Cool Head

Physiology ◽  
1986 ◽  
Vol 1 (2) ◽  
pp. 41-44 ◽  
Author(s):  
M Cabanac
Keyword(s):  
Heat Stress ◽  
Core Temperature ◽  
Heat Exchangers ◽  
The Body ◽  
Body Core Temperature ◽  
Mammalian Brain ◽  
Poor Tolerance ◽  
Selective Cooling ◽  
Body Core ◽  
The Brain

The mammalian brain has poor tolerance to increased temperature. However, when body core temperature rises during exercise or heat stress, the temperature of the brain can remain at a lower level, somewhat independent of the rest of the body. In several mammals the cooling of the brain is related to anatomically well-defined countercurrent heat exchangers. Humans lack these distinct anatomic structures, but significant cooling of the brain can nevertheless occur. Such selective cooling of the brain may have important medical implicantions.

Control of respiratory evaporative heat loss in exercising goats

1979 ◽  
Vol 46 (5) ◽  
pp. 978-983 ◽  
Author(s):  
J. B. Mercer ◽  
C. Jessen
Keyword(s):  
Heat Loss ◽  
Core Temperature ◽  
Heat Exchangers ◽  
The Body ◽  
Body Core Temperature ◽  
Evaporative Heat Loss ◽  
Hypothalamic Temperature ◽  
Body Core ◽  
Total Body ◽  
Rest And Exercise

Investigations were carried out to determine whether a nonthermal input is involved in the control of respiratory evaporative heat loss (REHL) in exercising goats. Two goats were implanted with hypothalamic perfusion thermodes and three goats were implanted with intravascular heat exchangers to clamp hypothalamic temperature and total body core temperature, respectively. At 30 degrees C air temperature REHL was measured while the animals were resting or walking on a treadmill (3 km.h-1, 5 degrees gradient). When the hypothalamic temperature was clamped between 33.0 and 43.0 degrees C the slopes of the responses relating increased REHL to hypothalamic temperature were similar during rest and exercise. However, the threshold hypothalamic temperatures for the increased REHL responses were lower during exercise than at rest, presumably due to higher extrahypothalamic temperatures. When the body core temperature was clamped between 37.0 and 40.4 degrees C the slopes of the responses relating increased REHL to total body core temperature during exercise showed only minor differences compared to those at rest, none of them conclusively indicating nonthermal influences.

Effects of estrogen on thermoregulatory evaporation in rats exposed to heat

1994 ◽  
Vol 267 (3) ◽  
pp. R673-R677 ◽  
Author(s):  
M. A. Baker ◽  
D. D. Dawson ◽  
C. E. Peters ◽  
A. M. Walker
Keyword(s):  
Heat Exposure ◽  
Plasma Osmolality ◽  
Ovariectomized Rats ◽  
Body Core Temperature ◽  
Temperature Sensitive ◽  
Sprague Dawley ◽  
Evaporative Water ◽  
Sprague Dawley Rats ◽  
Body Core ◽  
Opposite Order

The purpose of this study was to determine the effects of estrogen (E2) replacement on thermoregulation in ovariectomized rats exposed to heat. Female Sprague-Dawley rats were ovariectomized and splenectomized and implanted with a temperature-sensitive transmitter. Each rat was studied when E2 treated (after an E2 pellet implant) and untreated. Animals were divided into two groups with opposite order of treatment and were studied over a 9-wk period. Measurements of body core temperature (Tc) and evaporative water loss (EWL) were made on unrestrained animals resting at 38 degrees C air temperature. E2-treated animals increased EWL at all levels of Tc, reduced the threshold Tc for onset of saliva spreading, and regulated Tc at a lower level during heat exposure. E2 treatment elevated plasma E2 and reduced hematocrit but did not affect plasma osmolality. These effects of E2 on evaporative cooling and Tc in heat-stressed rats are similar to those that have been reported in human females. The mechanisms of the thermoregulatory effects of E2 remain to be studied.

Peripheral cholinergic pathway modulates hyperthermia induced by stress in rats exposed to open-field stress

2002 ◽  
Vol 92 (2) ◽  
pp. 789-794 ◽  
Author(s):  
Pamela Johnson Rowsey ◽  
Yong-Lu Yang ◽  
Christopher J. Gordon
Keyword(s):  
Open Field ◽  
Sprague Dawley ◽  
Cholinergic Mechanism ◽  
Antipyretic Effect ◽  
Field Stress ◽  
Induced Hyperthermia ◽  
Sprague Dawley Rats ◽  
Cholinergic Pathway ◽  
Hyperthermic Response ◽  
Methyl Scopolamine

Exposure to an open field is psychologically stressful and leads to an elevation in core temperature (Tc). Methyl scopolamine (MS), a muscarinic antagonist, and pyridostigmine (PYR), a carbamate that inhibits acetylcholinesterase, do not cross the blood-brain barrier and have little effect on Tc in resting, nonstressed animals. However, we have found that MS has an antipyretic effect on Tc that is caused by handling and cage-switch stress. PYR should act pharmacologically to reverse the effects of MS. To this end, we assessed the effects of MS and PYR on stress-induced hyperthermia. Male Sprague-Dawley rats at 90 days of age were housed individually at an ambient temperature of 22°C. Tc and motor activity were monitored by radiotelemetry in an open-field chamber. Rats were dosed intraperitoneally at 1200 with 1.0 mg/kg MS, 0.1 mg/kg PYR, a combination of MS and PYR, or saline and placed immediately inside the open-field chamber for 60 min. Stress-induced hyperthermia was suppressed immediately by MS and enhanced by PYR. Tc only increased by 0.3°C in the MS-treated animals. The hyperthermic response in the PYR group was nearly 0.6°C above that of rats dosed with saline. Coadministration of PYR and MS led to a stress-induced hyperthermia response nearly identical to that of rats injected with saline. Overall, open-field stress exacerbated the effects of MS and PYR on body Tc and provides support for a peripheral cholinergic mechanism that mediates stress-induced hyperthermia.

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